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Immunology Flashcards

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1
Q

What drug may be given along side corticosteroids to decrease the need for large doses of steroid

A

Azathioprine

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2
Q

Action of azathioprine

A

Inhibits DNA synthesis, inhibits T and natural killer cel functions and is anti-inflammatory

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3
Q

Action of cyclophosphamides

A

Interferes with DNA synthesis but has little anti-inflammatory activity and is therefore generally given in combination with steroid.

Useful in supressing B cell activity and antibody production (autoantibody in particular)

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4
Q

Actions of tacrolimus and cyclosporin

A

Involved in modulation and down-regulation of various genes, particularly transcription of interleukin 2; as a result major immune suppressive effects are on T cells and natural killer cells

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5
Q

Principal role of mycophenolic acid

A

Transplant rejection, crohn’s, and some systemic autoimmune diseases such as SLA, ITP, wegener’s

Prevents T cell proliferation, antibody production and leucocyte migration

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6
Q

What is cytokine receptor therapy designed to do

A

Inhibit the activity of harmful cytokines or enhance the activity of beneficial cytokines

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7
Q

How does plasma exchange work

A

Patient’s plasma is filtered off ex-vivo in a special cenrifycge apparatus; at the same time normal donor plasma is given back to the patient to replace what has been taken off.

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8
Q

When is immunoglobulin therapy appropriate

A

As replacement therapy in patients with primary or secondary antibody deficiency

As immune modulating therapy in certain inflammatory or autoimmune disorders e.g. Kawasaki’s, allergic disorders, vasculitis, myaesthenia, SLE, ITP, neuropathies

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9
Q

What are the adverse reactions associated with immunoglobulin therapy

A

Adverse reactions during infusions

Transmission of infection - particularly hep C

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10
Q

What kinds of transplant are available

A

Autograft - from same organism
Isograft - transfer from genetically identical members
Allograft - genetically non-identical members of the same species
Xenograft - transfer between species

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11
Q

What must donor and recipient share in order for a graft to survive

A

ABO blood group antigen and major histocompatability antigens (differing organs need different closeness)

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12
Q

Give an example of a priveledged site

A

Cornea

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13
Q

Why are grafts rejected

A

Histocompatability differences between donor and recipient

ABO mismatches are rare and usually due to human error; most are due to incomplete HLA matching

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14
Q

Which cells are part of the innate immunity

A

Phagocytes, eosinophils, basophils, mast cells, natural killer cells, actions of complement system

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15
Q

What are the markers of tissue inflammation

A

Red
Swollen
Heat
Pain

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16
Q

Cell mediated immunity

A

T cells are responsible

T helper cells and cytotoxic T cells

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17
Q

Which cells are responsible for humoral immunity

A

Antibodies/immunoglobulins secreted by plasma cells (formed from B cells)

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18
Q

What are the primary lymphoid tissues

A

Thymus

Bone marrow

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19
Q

What are the secondary lymphoid tissues

A

Lymph nodes, spleen, tonsils, adenoids, intestines/peyer’s patches, bone marrow

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20
Q

Which cells present class 1 HLA molecules

A

All nucleated cells - all except RBC

They present to cytotoxic t cells

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21
Q

Which cells present class 2 HLA molecules

A

Macrophages, b cells and macrophage like cells

They present to t helper cells

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22
Q

What makes CRP levels increase

A

Plasma concentrations are markedly increased during inflammation

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23
Q

What are interferons

A

A family of cytokines that non-specifically inhibit viral replication in host cells. In response to viral infection most cells secrete interferon

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24
Q

What is tolerance

A

The process whereby the immune system avoids producing damaging reactions against self antigens. It arises through deletion of autoreactive T and B cells during cell maturation (central tolerance) or by inhibiting the action which escape the central tolerance process

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25
Which immunoglobulins do babies gain from mothers
IgG from placenta IgA from milk
26
Aetiology of autoimmunity
Interaction of aetiological factors (genetic predisposition, immune regulatory factors, hormonal factors, environmental factors, aging, malignant disease, trauma...) in association with disordered and dysregulated immune effector mechanisms
27
Aetiology of autoimmunity
Genetic factors - inheritence of HLA types, familial predisposition Immune regulatory factors - defective tolerance induction, defective T cells, b cells Hormonal factors - female, high incidence onset during pregnancy, puberty, after starting OCP Environmental factors - infectious agents, solar radiation, drugs/chemicals, high fat diet, Other - malignant disease, ageing, trauma
28
Where are IgA immunoglobulins secreted
Plasma cells lining the respiratory, genito-urinary and gastro-intestinal tract And mammary glands
29
What are IgE antibodies mediated against
Allergy or multi-cellular parasites
30
Effector mechanisms involved in autoimmunity
Antibody (B cell) or cellular (T cell) activity Antibody and complement Immune complex formation Recruitment of innate components
31
Therapeutic options for autoimmunity
``` Immunosuppressive therapy Anti-inflammatory therapy Plasmapheresis (Bone marrow transplant) Replacement of lost physiological factor Organ/tissue/mechanical graft ```
32
What kind of hypersensitivity reaction is allergy
Type 1 - mediated by IgE
33
What is atopy
A genetic tendency to produce IgE to normally innocuous environmental allergens
34
What are the mast cell mediators
Preformed - histamine, heparin, tryptase... --> early phase response Newly synthesised - prostaglandins, leukotrienes --> late phase response
35
What is the effect of mast cells mediators
``` Mucosal oedema Capillary leakage Secretions Smooth muscle contraction Vasodilatation ```
36
Diagnosis of allergy
History!! Skin prick test Laboratory investigations - IgE levels = RAST test; can also test histamine, leukotriene, and tryptase
37
Treatment of allergy
Patient education and allergen avoidance Antihistamines - local or systemic Sodium cromoglycate - local (eye drops) or systemic Steroids - local/systemic Leukotriene antagonists Adrenaline epipen for anaphylaxis
38
Which immunoglobulins are implicated in type 2 hypersensitivity
IgG or IgM against self or exogenous
39
Haemolytic reaction following blood transfusion is a type __ hypersensitivity reaction
2 - mediated by IgM and IgG
40
Treatment of type 2 hypersensitivity
Prevention by cross matching of blood, tissue typing and detection of rhesus incompatibility in pregnancy Immune suppression in autoimmune disease and transplant rejection
41
Pathogenesis of type 2 hypersensitivity
Complement activation Fc uptake and stimulation of phagocytes Antibody dependent cellular cytotoxicity
42
Which organ specific autoimmune diseases are type 2 hypersensitivity reactions
Graves (against TSH receptor) Myaesthenia gravis (acetylcholine receptor) Good pastures syndrome (type IV collagen) Phemphigus (desmosomes)
43
In type 3 hypersensitivity reactions clinical conditions arise as a result of..
Abnormal deposition of immune complexes in tissues - may be a self or exogenous antigen Excessive or abnormal immune complex formation causes complement activation and recruitment and activation of inflammatory cells leading to tissue damage
44
What kind of hypersensitivity reaction is anaphylaxis
Type 1
45
What is serum sickness
A systemic illness where immune complexes form in the circulation and are deposited in a widespread fashion throughout many tissues - part of type 3 hypersensitivity
46
What is an arthus reaction
A localised disorder where complexes are formed locally in tissues
47
Precipitants of type 3 hypersensitivity reactions
Fungal antigens --> farmer's lung Avian antigens --> bird fancier's lung Complexes of streptococcal antigen and anti-strep antibody --> post streptococcal glomerulonephritis Leprosy, malaria, hepatitis (chronic infections) Tumours SLE
48
Treatment of type 3 hypersensitivity
Antigen elimination - infection or tumour Removal of immune complexes via plasma exchange/plasmaphoresis Immunosuppressive therapy
49
Which cells mediate type 4 hypersensitivity
Th1 cells and cytokine products
50
What do the cells mediating type 4 hypersensitivity react to
Inert environmental substances or as a reaction to infection with certain micro-organisms Reactions take place because immune system finds it difficult to destroy these environmental agents
51
Which hypersensitivity reaction is often delayed
Type 4 | Takes 48-72 hours
52
Clinical features of type 4 hypersensitivity
Tissue damage which occurs during microbial infections Mantoux test Contact dermatitis in response to metals, drugs, plastics, rubber, plants, cosmetics
53
Treatment of type 4 hypersensitivity (delayed type)
Avoidance or prevention of contact with antigens Corticosteroids Antimicrobial therapy as indicated by microorganisms
54
Cause of secondary immune deficiency
``` Malnutrition Malignant disease Splenectomy Infection Diabetes Burns/surgery Immunosuppressive therapy Chronic renal failure ```
55
Clinical presentation of phagocyte disorders
Pneumonia, osteomyelitis, skin/mucous membrane infection, liver abscesses, suppurating lymph nodes
56
What is hereditary angioedema
An autosomal dominant condition characterised by recurrent attacks of painless, non-pruritic, non-erythematous swellings in subcutaneous tissues, intestinal wall and larynx (due to deficiency f complement factor1)
57
Functions of the complement system
Inflammatory and chemotactic mediators Opsonins Membrane lysing complexes And maintaining solubility of circulating immune complexes
58
Clinical features of severe combines immune deficiency
``` Usually well for first 3 months of life Persistent superficial candida Diarrhoea and failure to thrive Chronic bronchiolitis Interstitial pneumonitis Overwhelming bacterial sepsis ```
59
Defects in____________ cause severe combines immune deficiency
Pluripotent stem cells Lymphoid stem cells T and B cells themselves
60
Management of severe combined immune deficiency
Intensive supportive therapy and nutritional support, prophylactic and therapeutic antibiotics, anti-fungal and anti-viral therapy prn and immunoglobulin replacement therapy Bone marrow transplant is curative
61
Presentation of IgA deficiency
Recurrent sinus and respiratory tract infections, GI disease, allergic symptoms and autoimmune disease
62
How could IgA deficiency be induced
Secondary to phenytoin, penicillamine, gold or sulphasalazine
63
Presentation of adaptive immune deficiency
``` Unexplained failure to thrive Excessive infections Abnormal lymphoid tissue Unexplained enlargement of liver or spleen Unexplained joint symptoms ```
64
Complications of adaptive immune deficiency
``` Infection - opportunistic, serious, persistent, unusual, recurrent Malignant disease Autoimmune disease Hypersensitivity disorders Iatrogenic problems ```
65
Infectious complications of antibody defects
Staph, strep, haemophilus, Giardia Echo and poliovirus
66
Infectious complications of T cell defects (e.g. In AIDS)
CMV, herpes, measles Mycobacteria, listeria Candida, aspergillus Pneumocystis, cryptosporidiosis, toxoplasma
67
General principles of treatment for immune deficiencies
``` Treat underlying cause if any Antimicrobial therapy AVOID IMMUNISATION WITH LIVE VACCINES AVOID BLOOD TRANSFUSION IN CELL MEDIATED DEFECTS Genetic counselling ``` Immunoglobulin replacement Thymic hormones Transplantation - bone marrow, fetal liver, fetal thymus Gene therapy Cytokine therapy
68
Main tests of humoral immunity
Immunoglobulin levels - serum/plasma of IgG,A,M,E
69
Main test for cell mediated immunity
T cell numbers Skin tests - should produce positive skin test in presence of normal T cell immunity against candida, tetanus, diptheria, mumps...
70
Effect of corticosteroids
Affect both T and B cell function. Major affects are on: cytokine networks, inflammation, T cell and monocyte function and transit and circulation of immunologically active cells.

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